title: Mechanisms for spontaneous termination of monomorphic, sustained ventricular tachycardia: results of activation mapping of reentrant circuits in the epicardial border zone of subacute canine infarcts.
abstract: OBJECTIVE
  The objective of this study was to determine why sustained ventricular tachycardias (VT) sometimes stop without outside intervention.
  
  
  BACKGROUND
  Sustained, monomorphic VT in patients with ischemic heart disease is often caused by reentrant excitation. These tachycardias can degenerate into rapid polymorphic rhythms or occasionally terminate spontaneously.
  
  
  METHODS
  Sustained VT was induced by programmed stimulation in dog hearts 4 to 5 days after ligation of the left anterior descending coronary artery. Activation in reentrant circuits in the epicardial border zone of the infarct was mapped using 192 to 312 bipolar electrodes.
  
  
  RESULTS
  Spontaneous termination of sustained VT always occurred when the reentrant wave front blocked in the central common pathway in reentrant circuits with a figure-of-eight configuration. Two major patterns of termination were identified from activation maps of the circuits that were not distinguishable from each other on the surface electrocardiogram: 1) Abrupt termination was not preceded by any change in the pattern of activation or cycle length. It could occur at different locations within the central common pathway, was not related to the directions of the muscle fiber orientation and was not caused by a short excitable gap. 2) Termination caused by premature activation (after a short cycle) either resulted from shortening of the functional lines of block around which the reentrant impulse circulated or was caused by wave fronts originating outside the reentrant circuit. In only one episode were oscillations of cycle length associated with termination.
  
  
  CONCLUSIONS
  The mechanisms for termination of reentry in functional circuits causing VT are different from those in anatomic circuits where oscillatory behavior precedes termination.
authors.affiliation: Department of Pharmacology, College of Physicians and Surgeons of Columbia University, New York, New York 10032, USA.
authors.forename: H
authors.initials: H
authors.lastname: Schmitt
authors.forename: A L
authors.initials: AL
authors.lastname: Wit
authors.forename: J
authors.initials: J
authors.lastname: Coromilas
authors.forename: B
authors.initials: B
authors.lastname: Waldecker
mesh_terms: D000818:Animals; D001283:Atrioventricular Node / Q000503:physiopathology; D018780:Body Surface Potential Mapping; D002304:Cardiac Pacing, Artificial; D003331:Coronary Vessels / Q000601:surgery; D004285:Dogs; D004558:Electric Stimulation; D004562:Electrocardiography; D006327:Heart Block / Q000503:physiopathology; D006339:Heart Rate / Q000502:physiology; D008026:Ligation; D018485:Muscle Fibers, Skeletal / Q000473:pathology; D009203:Myocardial Infarction / Q000473:pathology / Q000503:physiopathology*; D009206:Myocardium / Q000473:pathology; D010496:Pericardium / Q000473:pathology / Q000503:physiopathology*; D012075:Remission, Spontaneous; D012815:Signal Processing, Computer-Assisted; D013611:Tachycardia, Atrioventricular Nodal Reentry / Q000473:pathology / Q000503:physiopathology*; D017180:Tachycardia, Ventricular / Q000503:physiopathology*